Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.5.4.4 (adenosine deaminase)
5,136 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have previously shown that tuberculous pleurisy possesses a high level of adenosine deaminase (ADA) which is predominantly composed of ADA2. In this paper, we report the cases of tuberculous pleural effusion which contained mainly ADA1. In these cases, mycobacterium tuberculosis was positive by smear examination and/or culture and granulocytes were found to be major components. Analysis of lactate dehydrogenase (LDH) revealed that its activity was high and LDH5 occupied about 50% of total activity. In the tubercle bacillus negative cases, lymphocytes were the main components and the levels of LDH containing mostly LDH3 were low. It was assumed that the difference in LDH activity and isozyme pattern is due to the differential presence of leukocytes in pleurisy i.e., granulocytes and lymphocytes in tubercle bacillus positive and negative pleurisy, respectively. In conclusion, tuberculous pleural effusions can be divided into two groups on the basis of ADA and LDH activities and isozymes which may reflect the presence of mycobacterium tuberculosis.
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PMID:[Activities and isozymes of adenosine deaminase and lactate dehydrogenase in tuberculous pleural effusion with special reference to the presence of mycobacterium tuberculosis]. 130 Jan 8

We measured interleukin 6 (IL-6) concentrations in the pleural fluid of various patients to determine its role in pathophysiology and diagnosis by using specific functional bioassay. IL-6 levels were significantly higher in exudate than in transudate (79.3 +/- 176.2 U/ml [n = 55] vs 1.7 +/- 1.8 U/ml [n = 12]; p < 0.01). Tuberculous effusion contained a significantly higher amount of IL-6 than malignant effusion (181.3 +/- 176.2 U/ml [n = 13] vs 29.4 +/- 71.5 U/ml [n = 29]; p < 0.005). Pleural IL-6 levels were invariably higher than serum IL-6 levels, and both were significantly correlated (n = 21, r = 0.632; p < 0.02). Pleural IL-6 levels were significantly correlated with lactate dehydrogenase (LDH) in pleural fluid (r = 0.392; p < 0.01), ratio of pleural/serum LDH (r = 0.571; p < 0.01), pleural adenosine deaminase activity (r = 0.599; p < 0.01), and serum C-reactive protein (r = 0.494; p < 0.01). Furthermore, IL-6 levels were significantly correlated with peripheral blood platelet counts (r = 0.447; p < 0.001). These results suggest that (1) IL-6 is produced locally in pleural space, (2) pleural IL-6 level is helpful for differential diagnosis, and (3) locally produced IL-6 could leak to circulation and cause systemic effects such as the induction of C-reactive protein and thrombocytosis.
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PMID:Interleukin 6 activity in pleural effusion. Its diagnostic value and thrombopoietic activity. 139 42

A monoclonal antibody against soluble phase-terminal complement complex (SC5b-9) was used to try to differentiate pleural effusions of tuberculous vs malignant and other origin. Effusions of tuberculous origin showed a significantly higher SC5b-9 level than did plasma, suggesting activation of complement in the pleural space. All 26 patients with tuberculous effusions showed SC5b-9 levels in pleural fluid exceeding 2.0 mg/L, while 20 with malignant effusions had levels less than 2.0 mg/L. However, rheumatoid, some parapneumonic, and treated malignant effusions showed SC5b-9 levels above 2.0 mg/L. Considering a value exceeding 2.0 mg/L, the specificity and sensitivity of the SC5b-9 estimation in tuberculosis were 0.74 and 1.0, respectively. The mean values for C4d and Bb fragments of complement were significantly (p < 0.05) higher in the tuberculous than in the malignant effusions. However, the values for Bb in 16 (62 percent) of the 26 patients with tuberculous or malignant effusions were in the same range. The activity of adenosine deaminase (ADA) was higher in the tuberculous than in the malignant effusions. While 18 of 26 patients with tuberculous effusions showed an ADA value exceeding 50 mU/ml, the estimated cutoff point (sensitivity = 0.69), 35 of the 36 nontuberculous effusions showed a true negative value (specificity = 0.97). A correlation between ADA and SC5b-9 values was observed in pleural effusions. These observations suggest that the estimation of SC5b-9 in pleural fluid presents a new approach to differentiating tuberculous vs malignant effusions.
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PMID:Pleural SC5b-9 in differential diagnosis of tuberculous, malignant, and other effusions. 139 43

The aim of this study was to confirm that ascitic fluid determination of adenosine deaminase activity (ADA) is useful for the diagnosis of tuberculous peritonitis. 109 patients with ascites have been studied; 4 had tuberculous peritonitis and 105 nontuberculous ascites. The mean value of ascitic fluid AQDA was 0.587 +/- 0.2 uKat/l in tuberculous peritonitis and 0.11 +/- 0.1 uKat/l in nontuberculous ascites (p less than 0.001). An ADA value upper than 0.40 uKat/l has a sensitivity of 100% and a specificity of 99% for diagnosing tuberculous peritonitis. Ascitic fluid determination of ADA is simple, cheap and has a good diagnostic accuracy. In countries with high incidence of tuberculosis, measurement of ADA in ascitic fluid should be used as screening test for tuberculosis.
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PMID:[The value of ADA in peritoneal tuberculosis]. 152 May 47

Human adenosine deaminase (ADA; EC 3.5.4.4) consists of three isoenzymes: ADA1, ADA1+CP, and ADA2. We developed an electrophoretic technique to distinguish between these three isoenzymes. The isoenzyme pattern was studied in tissue and cell homogenates, as well as in serum from normal subjects and from patients with increased serum ADA who had either hepatitis, infectious mononucleosis, tuberculosis, pneumonia, rheumatoid arthritis, or acute lymphoblastic leukemia (ALL). The highest ADA activity was found in lymphocytes and monocytes. ADA2 could be detected only in monocytes (18% of total ADA activity). It was also the predominant isoenzyme in the sera of controls and all disease groups, except for ALL--the only condition evaluated that is not of an inflammatory nature. We conclude that serum ADA reflects monocyte/macrophage activity or turnover in most diseases studied. The exception is ALL, where serum ADA most probably originates from lymphocyte precursors.
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PMID:Serum adenosine deaminase: isoenzymes and diagnostic application. 162 98

The value of ascites gamma interferon concentration and ascites adenosine deaminase activity in distinguishing tuberculosis from other causes of ascites was examined in a prospective study of 86 patients with ascites, including 16 with tuberculous peritonitis. Gamma interferon concentration was higher in tuberculous peritonitis than in the other causes of ascites (p less than 0.0001), and a cut-off between 3 and 9 u/ml reached a sensitivity and a specificity of 100%. The mean (+/- SD) gamma interferon level in tuberculous ascites was 39.3 +/- 18.3 u/ml in patients seronegative for HIV and 14.2 +/- 4.7 u/ml in patients with AIDS (p = 0.01). Adenosine deaminase activity in tuberculous ascites was also higher than in the other causes of ascites (p less than 0.0001), and a cut-off of 40 u/l reached a sensitivity of 100% and a specificity of 97%. The two false positives for adenosine deaminase test were true negatives for the gamma interferon test. There was no significant correlation between gamma interferon concentration and adenosine deaminase activity either in tuberculous ascitis or in any other group. This study suggests that ascites gamma interferon determination may be very useful in the screening of tuberculous peritonitis, but its cost makes it advisable to use adenosine deaminase activity as a routine test, at least in areas where tuberculosis is endemic.
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PMID:Diagnostic value of ascites gamma interferon levels in tuberculous peritonitis. Comparison with adenosine deaminase activity. 177 79

Adenosine deaminase is an enzyme that actively participates in the metabolism of the adenine nucleotides. It catalyzes the irreversible hydrolytic deamination of deoxyadenosine and adenosine with the production of deoxyinosine and inosine respectively and of ammonia. This enzyme thus plays an important role in lympho-monocyte maturation and activation. The increase in its activity in different biological fluids (pleural, pericardial, peritoneal, intra-articular and cerebrospinal fluids) has been used as a rapid diagnostic test in tuberculosis infection. In human immunodeficiency virus infection, it was verified that enzymatic activity progressively increases in serum and blood cells, accompanying the natural evolution of the disease. The physiopathological mechanism has not been definitely established but the CD4+ lymphocytes and macrophages are pointed to as being accountable for the enzyme's increase in activity. For this reason, adenosine deaminase could be a marker of the cellular immune response. The study of adenosine deaminase activity in blood cells elucidated the diagnosis of severe combined immunodeficiency (due to a congenital lack of the enzyme) in 30 to 50% of the cases. One type of congenital hemolytic anemia is due to an exaggerated enzymatic activity in red blood cells.
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PMID:[Adenosine deaminase. A pluridisciplinary enzyme]. 180 98

The activity of adenosine deaminase in the pleural fluid of 218 consecutive patients was studied. According to the etiology of exudative pleural effusions, the patients were divided into the following five groups: (1) tuberculosis; (2) lung cancer; (3) pneumonias; (4) miscellaneous; and (5) idiopathic. Patients with pleural tuberculosis presented significantly higher ADA activity than patients with nontuberculous pleural effusions (p less than 0.0001). The results indicated that in a population with a relatively high prevalence of tuberculosis, the analysis of ADA levels in pleural effusions constitutes a useful marker for the diagnosis which, in addition, can be made quickly and cheaply. Additionally, a comprehensive review of the literature on the role of ADA in the diagnosis of tuberculous pleural effusions is presented.
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PMID:Adenosine deaminase in the diagnosis of tuberculous pleural effusions. A report of 218 patients and review of the literature. 162 88

A prospective study of 111 adult patients with a pleural effusion was carried out in an area with a high prevalence of tuberculosis to compare the yield of bedside with laboratory inoculation of pleural fluid, and the yield and speed of a radiometric mycobacterial culture system (BACTEC) with that of conventional culture. The use of adenosine deaminase activity in pleural fluid as a diagnostic test for tuberculosis was also evaluated. In the 62 cases of tuberculosis confirmed histologically or by culture, or both, the BACTEC system had the same culture yield as conventional mycobacterial culture (positive in 14 cases-23%), but was significantly faster (18 versus 33 days). Bedside inoculation had a culture yield significantly higher than laboratory inoculation in the 24 patients tested (11 versus four). The remaining three diagnostic categories were malignant (28), miscellaneous (10), and undiagnosed (11). Median adenosine deaminase activity was significantly higher in tuberculous effusions than in any of the other categories, but there was considerable overlap between the groups. It is concluded that the BACTEC system is significantly faster than conventional mycobacterial culture and that bedside inoculation of pleural fluid substantially increases culture yield. Adenosine deaminase does not provide as valuable a diagnostic test of pleural tuberculosis as has been suggested.
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PMID:Tuberculous pleural effusions: increased culture yield with bedside inoculation of pleural fluid and poor diagnostic value of adenosine deaminase. 190 72

Tuberculous pleurisy is a good model for resolution of local cellular immunity. It would be expected that tuberculous pleural fluid contains a variety of immunologically important cytokines because of the accumulation of immunocompetent cells in the pleural cavity. We studied interleukin 1 (IL-1), interleukin 2 (IL-2), and interferon gamma (IFN-gamma) levels in pleural fluid of 20 patients with tuberculous pleurisy and compared them with those in pleural fluid of 20 patients with malignant pleurisy. We also evaluated adenosine deaminase (ADA) levels in both effusions. Tuberculous pleural fluid had higher levels of IL-1, IL-2, IFN-gamma, and ADA than malignant pleural fluid. Although the difference of IL-1 level between tuberculous and malignant pleural fluid was modest, that of IL-2, IFN-gamma, and ADA was dominant. These findings suggest that activated T lymphocytes in tuberculous pleural fluid concern the production of lymphokines at the morbid site and they effectively exert local cellular immunity through the action of such lymphokines.
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PMID:Cytokine content in pleural effusion. Comparison between tuberculous and carcinomatous pleurisy. 190 58


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